Volatile anesthetics decrease myocardial contractility independently of sarcoplasmic reticulum Ca2+ release, with no significant differences between halothane, isoflurane, and sevoflurane.
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Should not yet inform clinical anesthetic selection; extends mechanistic evidence for SR-independent effects in animal models.
The volatile anesthetics halothane, isoflurane, and sevoflurane depress myocardial contractility by decreasing transsarcolemmal Ca2+ influx, Ca2+ release from the sarcoplasmic reticulum, Ca2+ sensitivity of the contractile proteins, and cross-bridge performance. The aim of this study is to assess and compare the effects of halothane, isoflurane, and sevoflurane on contractility in conditions in which sarcoplasmic reticulum Ca2+ release is abolished by pretreatment with ryanodine. Ferret right ventricular papillary muscles were exposed to ryanodine at 10(-6) M and then to incremental concentrations of halothane, isoflurane, or sevoflurane. In the presence of ryanodine, each anesthetic decreased isometric and isotonic contractility in a reversible, concentration-dependent manner with no differences between anesthetics and with little or no effect on time variables. It is likely that differences between anesthetic effects on contraction amplitude in isometric and isotonic twitches reside in their effects on the sarcoplasmic reticulum.
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Housmans et al. (2001) studied this question.
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